CLN7 neuronal ceroid lipofuscinosis is an inherited lysosomal storage neurodegenerative disease highly prevalent in children.
In her webinar, Dr García Macía discusses how failure in autophagy causes the accumulation of structurally and bioenergetically impaired neuronal mitochondria in the mouse model of CLN7 disease, and how the mitochondrial reactive oxygen species (mROS) in Cln7 disease neurons mediates glycolysis activation and contributes to CLN7 pathogenesis.
Tune in to learn more about:
- Neuronal metabolism
- How mitochondria are affected in a lysosomal storage disease
- How modulating ROS and metabolism may advance therapeutic discoveries for neurodegeneration